A curious case of ovarian cysts.

ABSTRACT: Benign mature cystic teratomas are a form of ovarian germ cell tumor that originates from primordial germ cells in the ovaries. Of the three types of teratoma neoplasms, benign mature cystic teratomas (also called dermoid cysts) are the most common. Patients may present with intermittent abdominal or pelvic pain, abdominal enlargement, dysmenorrhea, dyspareunia, or may be asymptomatic. Clinicians should have a high suspicion for benign mature cystic teratomas, which account for more than 20% of all ovarian neoplasms. This article focuses on the clinical symptoms, ovarian growth characteristics, pathophysiology, potential complications, management options, and recurrence of benign mature cystic teratomas.

Stochastic Expression of Sae-Dependent Virulence Genes during Staphylococcus aureus Biofilm Development Is Dependent on SaeS.

The intricate process of biofilm formation in the human pathogen Staphylococcus aureus involves distinct stages during which a complex mixture of matrix molecules is produced and modified throughout the developmental cycle. Early in biofilm development, a subpopulation of cells detaches from its substrate in an event termed "exodus" that is mediated by SaePQRS-dependent stochastic expression of a secreted staphylococcal nuclease, which degrades extracellular DNA within the matrix, causing the release of cells and subsequently allowing for the formation of metabolically heterogenous microcolonies. Since the SaePQRS regulatory system is involved in the transcriptional control of multiple S. aureus virulence factors, the expression of several additional virulence genes was examined within a developing biofilm by introducing fluorescent gene reporter plasmids into wild-type S. aureus and isogenic regulatory mutants and growing these strains in a microfluidic system that supplies the bacteria with a constant flow of media while simultaneously imaging developing biofilms in 5-min intervals. This study demonstrated that multiple virulence genes, including nuc, were expressed stochastically within a specialized subpopulation of cells in nascent biofilms. We demonstrated that virulence genes regulated by SaePQRS were stochastically expressed in nearly all strains examined whereas Agr-regulated genes were expressed more homogenously within maturing microcolonies. The commonly used Newman strain contains a variant of SaeS (SaeSP) that confers constitutive kinase activity to the protein and caused this strain to lack the stochastic expression pattern observed in other strain backgrounds. Importantly, repair of the SaeSP allele resulting in reversion to the well-conserved SaeS L allele found in other strains restored stochastic expression in this strain.IMPORTANCEStaphylococcus aureus is an important human pathogen capable of colonizing diverse tissue types and inducing severe disease in both immunocompromised and otherwise healthy individuals. Biofilm infections caused by this bacterial species are of particular concern because of their persistence, even in the face of intensive therapeutic intervention. The results of the current study demonstrate the stochastic nature of Sae-mediated virulence gene expression in S. aureus and indicate that this regulatory system may function as a "bistable switch" in a manner similar to that seen with regulators controlling competence gene expression in Bacillus subtilis and persister cell formation in Escherichia coli The results of this study provide a new perspective on the complex mechanisms utilized by S. aureus during the establishment of infections.

Enzyme linked immunosorbent assay for quantification of bovine interleukin-8 to study infection and immunity in the female genital tract.

PROBLEM: The chemokine IL-8 recruits neutrophils to sites of infection, including the endometrium of the bovine uterus. However, quantification of bovine IL-8 often yields lower concentrations than for other species, which may reflect impaired innate immune responses by bovine cells or inaccurate measurement of IL-8 using the current human IL-8 ELISA method. METHOD OF STUDY: An ELISA was developed and validated for detection of bovine IL-8. Utility of the assay was tested by measuring the response of bovine endometrium and cells to bacteria and pathogen-associated molecular patterns. RESULTS: The developed ELISA detected 62.5-2000 pg/mL IL-8, with minimal cross-reactivity to other inflammatory mediators. Concentrations of bovine IL-8 were measured more accurately by the bovine than human IL-8 ELISA. Bovine endometrial IL-8 responses to pathogen-associated molecules were quantitatively similar to other species. CONCLUSION: A bovine-specific IL-8 ELISA was developed, which accurately measured IL-8 secretion from endometrial cells.

Severity of lung injury in cyclooxygenase-2-deficient mice is dependent on reduced prostaglandin E(2) production.

Levels of prostaglandin E(2) (PGE(2)), a potent inhibitor of fibroblast function, are decreased in the lungs of patients with pulmonary fibrosis, which has been shown to be because of limited expression of cyclooxygenase-2 (COX-2). To further investigate the relative importance of COX-2 and PGE(2) in the development of fibrosis we have used a selective COX-2 inhibitor and COX-2-deficient ((-/-) and (+/-)) mice in studies of bleomycin-induced lung fibrosis. We demonstrate in wild-type mice that bleomycin-induced lung PGE(2) production is predominantly COX-2 mediated. Furthermore, COX-2(+/-) mice show limited induction of PGE(2) and an enhanced fibrotic response with increased lung collagen content compared with wild-type mice after bleomycin injury (P < 0.001). In contrast, COX-2(-/-) mice show increased levels of lung PGE(2), compared with wild-type mice after injury (P < 0.05), because of compensatory up-regulation of COX-1, which appears to be associated with macrophage/monocytes but not fibroblasts derived from these mice. COX-2(-/-) mice show an enhanced and persistent inflammatory response to bleomycin, however the fibrotic response to injury was unaltered compared with wild-type animals. These data provide further direct evidence for the importance of up-regulating COX-2 and PGE(2) expression in protecting against the development of fibrosis after lung injury.